Neurons cell membrane

Substances from different chemical classes suspend consciousness when given intravenously and can be used as injectable anesthetics (B). Unlike inha-lational agents, most of these drugs affect consciousness only and are devoid of analgesic activity (exception ketamine). The effect cannot be ascribed to nonselective binding to neuronal cell membranes, although this may hold for propofol... 

The composition of the cell membrane varies from one anatomical location to another. For example, the cell membranes of neurons are 75% lipid and 25% protein, while those of epithelial cells in the intestinal villi are 75% protein and 25% lipid. The mixture of lipids that constitutes the cell membranes of neurons is different from that found in other organ systems the same applies to the membrane proteins of neurons. Cell membranes are dynamic structures the phospholipids and fatty acids are in a state of constant turnover the protein components tend to turnover with a cycle ranging from 9 days to 6 months. 

In contrast to that observed in the heart, histamine H3-receptors in vessels may be located at neuronal, as well as non-neuronal cell membranes. Three different localisations, prejunctional, endothelial and post-junctional (muscular cell) level have been found. A synopsis of the results obtained in vessels is depicted in Table 8. 

Potassium bromide appears to stabilize neuronal cell membranes by interfering with chloride ion transport across them. It potentiates the effect of GABA by hyperpolarizing the membrane. Other drugs with GABAergic activity, such as the barbiturates, may act synergistically with potassium bromide to raise the seizure threshold. 

Lithium is similar to sodium in that it forms positive ions (Li+) and can pass through sodium ion channels in neuronal cell membranes. It tends to accumulate inside neurons and may interfere with nerve action potentials or the activation of second messenger systems within the neuron (see Chapter 3, page 63). In addition, lithium may inhibit the release of monoamines from nerve endings and increase their uptake. However, the exact mode of action of lithium in affective disorders is unknown. 

The mechanism of action of general anaesthetics is unknown, but there are two theories to explain their action the lipid theory and the protein theory. The lipid theory states that general anaesthetics interact with lipids in the neuronal cell membrane and disrupt neurotransmission and the protein theory states that general anaesthetics interact with membrane proteins to alter release of neurotransmitters. The protein theory is thought most likely. 

Ethanol acts to increase the fluidity of neuronal cell membranes, potentiate the conformational changes of the GABA receptor, and increase chloride flux across the membrane. This results in decreased excitability of the membrane. 

Neuronal membranes contain phospholipids. A lack of essential fatty acids, such as omega-3 fats, or excessive intake of saturated fats, margarine, cholesterol, and animal fatty acids, can result in abnormalities. The neuronal cell membrane regulates the passage of molecules into and out of the cell. Neuronal membrane fluidity is believed to impact behavior, mood, and mental function. Physical properties, including the fluidity, of neuronal membranes affect neurotransmitter synthesis, signal transmission, uptake of serotonin and other neurotransmitters, neurotransmitter binding, and the activity of key enzymes that break down neurotransmitters like serotonin, epinephrine, dopamine, and norepinephrine. 

These glycolipids form a large fraction of neuronal cell membranes, and defects in their metabolism leads to a series of devastating diseases, the best known of which is Tay-Sachs. The compounds are synthesized from the lipid ceramide by successive addition of monosaccharides (Figure 21.14), where the numbers in boxes correspond to the E.C. number for the enzyme responsible... 

Normal PrP protein is anchored to the neuronal cell membrane by a GPI linkage. Disabhng the GPI linkage in transgenic mice does not prevent the accumulation of PrF plaques in inoculated mice, but does prevent the development of scrapie disease (Chesebro et al., 2005). 

Neural Excitation of Muscle. Voluntary contraction of human muscle initiates in the frontal motor cortex of the brain, where impulses from large pyramidal cells travel downward through corticospinal tracts that lead out to peripheral muscles. These impulses from the motor cortex are called action potentials, and each impulse is associated with a single motor neuron. The principle structure of a motor neuron is shown in Fig. 6.IS. The action potential initiates in the cell body, or soma, and travels down a long efferent trunk, called the axon, at a rate of about 80 to 120 m/s. The action potential waveform is the result of a voltage depolarization-repolarization phenomenon across the neuron cell membrane. The membrane ionic potential at rest is distuibed by a surrounding stimulus, and Na ions are allowed to momentarily rush inside. An active transport mechanism, called the Na —K+ pump, quickly returns the transmembrane potential to rest This sequence of events, which lasts about 1 ms, stimulates a succession of nerve impulses or waves that eventually reach muscle... 

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